Spinal cord synapses stabilized by glatiramer acetate.

MS Breakthrough: Can Glatiramer Acetate Stabilize Spinal Synapses?

Jordan Keane in Health & Wellness November 2025 • 4 min read.

"New research explores how glatiramer acetate (GA) treatment impacts spinal synapse stability and MHC I regulation in experimental autoimmune encephalomyelitis (EAE), offering hope for multiple sclerosis (MS) treatment."

Multiple sclerosis (MS) is a chronic autoimmune disease affecting millions worldwide. It is characterized by the immune system attacking the protective myelin sheath around nerve fibers in the brain and spinal cord, leading to a wide range of neurological symptoms. While there is currently no cure for MS, various treatments aim to manage symptoms and slow disease progression.

One such treatment is glatiramer acetate (GA), also known as Copaxone, an immunomodulatory drug. GA has been used for decades to treat relapsing-remitting MS, one of the most common forms of the disease. While its exact mechanism of action remains under investigation, GA is believed to work by altering the immune response and reducing inflammation in the central nervous system (CNS).

Recent research has shed light on a new potential mechanism by which GA may exert its beneficial effects. This research focuses on the role of major histocompatibility complex class I (MHC I) molecules in synaptic plasticity, the brain's ability to reorganize itself by forming new neural connections throughout life. Emerging evidence suggests that MHC I molecules, traditionally known for their role in the immune system, also play a role in synaptic elimination, the process of pruning synapses to refine neural circuits.

How Does Glatiramer Acetate Impact Spinal Synapses?

Spinal cord synapses stabilized by glatiramer acetate.

A study published in the International Journal of Biological Sciences investigated how GA treatment influences MHC I expression and synaptic plasticity in the spinal cord during experimental autoimmune encephalomyelitis (EAE). EAE is an animal model of MS, mimicking the inflammation and demyelination seen in the human disease. Researchers induced EAE in C57BL/6J mice and then treated them daily with either GA or a placebo. The mice were sacrificed at two time points: the peak of the disease (14 days after induction) and during the recovery phase (21 days after induction).

The spinal cords were then examined using a variety of techniques, including immunohistochemistry, Western blotting, and transmission electron microscopy. These methods allowed the researchers to assess MHC I expression, the presence of synaptic proteins, and the overall structure of synapses.

Here’s what they discovered:

Reduced Synaptic Loss: GA treatment was associated with decreased synaptic loss during EAE.
Downregulation of MHC I: The reduction in synaptic loss correlated with the downregulation (reduction) of MHC I expression in the spinal cord.
Neuroprotective Role: These findings reinforce the idea that GA has a neuroprotective role, preserving synapses from damage during the course of the disease.

Essentially, the study suggests that GA may help to stabilize spinal synapses in MS by influencing the expression of MHC I molecules. This is important because synapse loss is thought to contribute to the neurological deficits seen in MS.

Looking Ahead: What Does This Mean for MS Treatment?

This research provides valuable insights into how glatiramer acetate may work to protect the nervous system in multiple sclerosis. By demonstrating that GA can influence MHC I expression and stabilize synapses, the study opens new avenues for understanding and potentially improving MS treatments. Future research should focus on further elucidating the precise mechanisms by which GA interacts with MHC I and other molecules involved in synaptic plasticity. Clinical trials may also be warranted to investigate whether these findings translate into improved outcomes for MS patients.

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This article is based on research published under:

DOI-LINK: 10.7150/ijbs.7.1188, Alternate LINK

Title: Glatiramer Acetate Treatment Increases Stability Of Spinal Synapses And Down Regulates Mhc I During The Course Of Eae

Subject: Cell Biology

Journal: International Journal of Biological Sciences

Publisher: Ivyspring International Publisher

Authors: Juliana M. Scorisa, Camila M. Freria, Sheila C. Victorio, Roberta Barbizan, Renata G. Zanon, Alexandre L. R. Oliveira

Published: 2011-01-01

Everything You Need To Know

What is the primary function of Glatiramer Acetate (GA) in the context of Multiple Sclerosis (MS)?

Glatiramer Acetate (GA), also known as Copaxone, is an immunomodulatory drug used to treat relapsing-remitting MS. Its primary function is to alter the immune response and reduce inflammation within the central nervous system (CNS). Recent research suggests GA may also stabilize spinal synapses by influencing the expression of Major Histocompatibility Complex class I (MHC I) molecules, offering neuroprotection.

How does Glatiramer Acetate (GA) affect Major Histocompatibility Complex class I (MHC I) in the spinal cord?

The study indicates that Glatiramer Acetate (GA) treatment leads to a downregulation, or reduction, of Major Histocompatibility Complex class I (MHC I) expression in the spinal cord. This reduction correlates with decreased synaptic loss during Experimental Autoimmune Encephalomyelitis (EAE), an animal model of Multiple Sclerosis (MS). By influencing MHC I expression, GA appears to stabilize synapses, potentially mitigating the neurological deficits associated with MS.

In the context of MS, what is the significance of synaptic loss, and how does Glatiramer Acetate (GA) address it?

Synaptic loss, the loss of connections between nerve cells, is believed to contribute significantly to the neurological deficits observed in Multiple Sclerosis (MS). Glatiramer Acetate (GA) has been shown to reduce synaptic loss. GA's neuroprotective role helps preserve synapses from damage by influencing the expression of Major Histocompatibility Complex class I (MHC I) molecules, thus potentially slowing the progression of neurological symptoms associated with MS.

What is Experimental Autoimmune Encephalomyelitis (EAE), and why is it relevant to the study of Glatiramer Acetate (GA) for Multiple Sclerosis (MS)?

Experimental Autoimmune Encephalomyelitis (EAE) is an animal model of Multiple Sclerosis (MS). It mimics the inflammation and demyelination seen in human MS, allowing researchers to study the disease process and test potential treatments. In the study, EAE was induced in C57BL/6J mice to investigate how Glatiramer Acetate (GA) affects MHC I expression and synaptic plasticity in the spinal cord. The results from this model provide insights into GA's neuroprotective mechanisms and its potential benefits in MS.

Beyond the stabilization of spinal synapses, what other potential benefits does Glatiramer Acetate (GA) offer in the treatment of Multiple Sclerosis (MS), and what future research is suggested?

Besides stabilizing spinal synapses, Glatiramer Acetate (GA) offers the potential to protect the nervous system by influencing Major Histocompatibility Complex class I (MHC I) expression. Future research should focus on precisely how GA interacts with MHC I and other molecules involved in synaptic plasticity. Clinical trials are also suggested to investigate whether these findings translate to improved outcomes for Multiple Sclerosis (MS) patients. The ultimate goal is to improve current treatments by understanding and enhancing the drug's effect.